The mechanisms that mediate the neurocognitive consequences of pediatric OSA includes intermittent hypoxia, arousal and sleep fragmentation besides the evolving role of a molecular basis responsible for end-organ damage including many recently studied biomarkers as plasma insulin growth factor-1 (IGF-1) plasma IL-6 and high-sensitivity C-reactive protein urinary neurotransmitters urinary catecholamines, taurine and GABA [6]. This evidence concerns the gene IL6 and obstructive sleep apnea syndrome.